There are three main findings in the present study. First, 27.2% of the patients had abnormal EEG recordings and 12.3% had abnormal MRI scans. This result supports the importance of EEG and MRI evaluations in this population. However, Kawasaki et al
reported higher rates (up to 60%) of EEG abnormalities in autistic subjects. The lower levels of EEG abnormalities in our study might be due to the younger age of the sample (aged 6 or younger, 53.1%). It is known that seizures are more prevalent in adolescents and young adult patients.
In fact, patients with EEG abnormalities were significantly older in our study. Besides, over 60% of patients in the study by Kawasaki et al
had severe mental retardation, but only 25% of our patients were severely intellectually disabled. We did not find any association between MRI abnormalities and the severity of ID. This might be due to the low power of the study with small sample size.
We found the relation of abnormal EEG recordings with ID. Approximately half of the patients with severe ID had EEG abnormalities, but only 8.3% of the non-ID patients had EEG abnormalities. This finding is consistent with that of previous studies.[1,17]
Therefore non-ID subjects with pervasive developmental disorders might have more preserved neural functions. As shown in Fig., mild and moderate ID patients had higher rates of EEG abnormalities than non-ID patients, but severe ID patients had a higher rate of EEG abnormality than milder ID patients, suggesting that the association of EEG abnormalities with ID could be “severity-dependent”. This is also consistent with previous studies which have shown that the risk of epilepsy increases significantly in patients with severe ID.
Thus, the frequency of abnormal EEG in PDD patients may be attributable to ID status, as in individuals without PDD.
Our results suggest that consistent with previous literature, patients with PDD frequently have EEG and MRI abnormalities. However, when patients without MRI abnormalities were analyzed, the rate of EEG abnormalities remained the same and the relation with ID persisted. The findings suggest that EEG abnormalities in patients with PDD are frequent both with and without MRI structural abnormalities.
MRI abnormalities detected in 12.3% of the patients were mild cortical atrophy and bilateral periventricular leukomalacia. EEG abnormalities detected were focal active epileptic and paroxysmal abnormalities which were frequently detected in the right and left temporal cortex and adjacent cortical structures. The findings are consistent with previous studies,[3,18]
suggesting that focal and multifocal paroxysmal EEG abnormalities are common in the centro-parieto-temporal regions, and that temporal cortex might play an important role in the pathophysiology of autism. Joint attention deficit in autism, which is a core symptom, may be related to medial temporal lobe dysfunction.
Single photon emission computed tomography and positron emission tomography studies also suggest medial temporal lobe involvement.[20,21]
In tuberous sclerosis, a hereditary neurocutaneous syndrome associated with a high incidence of autism, symptoms of autism are strongly related to the presence of tubers and epileptiform discharges in the temporal lobe.[22,23]
Brain regions other than the temporal cortex have been implicated in autism. Postmortem and neuroimaging studies have found abnormalities in the anterior cingulate cortex,
and facial nucleus.
However, these studies were conducted with pure autistic subjects; therefore, it may not be possible to generalize the findings to all PDD patients.
Frequent MRI abnormalities were mild cortical atrophy and bilateral periventricular leukomalacia, which could be related to hypoxic-ischemic encephalopathy. This is consistent with previous studies.
This result might support the idea that birth trauma and related hypoxia might be an important cause of pervasive developmental disorders.
We did not find significant differences in the frequency of EEG and MRI abnormalities in patients with or without obstetric complications; however, the use of parental history to obtain information about obstetric complications might be inaccurate. Moreover, not every of hypoxic births results in PDD, suggesting that obstetric complications might trigger an existing vulnerability in PDD patients. The type of MRI pathology was not related to a history of obstetric complication history, although the sample for this analysis was very small.
There are limitations in this study. Since this study is retrospective, a uniform diagnostic method for establishment of a PDD diagnosis was not used. In summary, almost a fourth of the patients with pervasive developmental disorders had EEG or MRI abnormalities, and the rate of EEG abnormalities has a severity-dependent relation with ID. The most frequent MRI abnormalities might be related to hypoxic-ischemic encephalopathy, and temporal cortex and adjacent cortical structures are the most frequent sites of local active epileptic and paroxysmal EEG abnormalities.